In assessing mechanisms by which environmental contaminants might exert toxic effects on living cells, one looks for sites which are both readily accessible and functionally important. The membrane theory of toxicity fits both criteria, i.e., the cell membrane is the first barrier met by toxic agents reaching a cell and the selective permeability characteristics of this membrane are vital for regulation of cell volume and ionic composition, for entry of nutrients and elimination of wastes, and in excitable cells, for initiation and conduction of the action potential. Likewise, overall homeostasis in multicellular organisms depends upon the same membrane transport functions in epithelial cells of many tissues including intestine, kidney, and accessory organs, e.g., gill and nasal gland. Furthermore, even at the level of subcellular organelles, membrane integrity is essential for vital processes such as oxidative phosphorylation in mitochondria. The immediate objective is a comprehensive physiological- biochemical- morphological evaluating of the effects of heavy metal, petroleum and organochlorine pollutants on osmoregulatory and nutritive membrane functions in selected species of aquatic birds and fish. Our decision to focus on these particular aspects of membrane toxicity is based, in part, on fragmentary data from our and other laboratories already suggesting disruption of osmoregulatory and/or nutritive transport in these species. The long-term objective is to evaluate the role of altered membrane transport as one of the primary mechanisms by which various pollutants exert toxic effects on living cells. The cell membrane theory of toxicity offers a rational approach to 1) explaining toxicities of known pollutants, 2) designing indicator tests for environmental warning, and 3) predicting future health hazards including synergistic actions. For example, we have successfully explained a classical environmental warning, DDT-induced eggshell thinning, by evaluating toxic effects on calcium transport in avain shell gland epithelium.